Abstract
The study explores how activating autophagy in yellow catfish under chronic ammonia stress (CAS) can boost growth and improve ammonia detoxification, addressing the serious threat of ammonia stress on fish survival and disease susceptibility in aquatic settings. Yellow catfish (Pelteobagrus fulvidraco) weighing 2.35 ± 0.13 g were divided into three groups over an 8-week period: CON group without ammonia exposure, AM group exposed to 50 mg/L total ammonia nitrogen (T-AN), and AM+RAPA group fed diets with 3 mg/100 g rapamycin under 50 mg/L T-AN. Dietary rapamycin (DR) can alleviate growth retardation, liver structural damage, inflammation, apoptosis, decreased detoxification capacity, and reduced survival rate caused by CAS. Additionally, DR can mitigate autophagy inhibition induced by CAS. Metabolomics analysis revealed that activation of autophagy by DR significantly alleviated the glutamate, aspartate n-acetyl-l-glutamate, ornithine, argininosuccinate, and citrulline levels in the liver induced by CAS. This suggests that autophagy activation can supplement these metabolites involved in urea and glutamine synthesis, thereby promoting ammonia detoxification. In conclusion, liver autophagy is a vital mechanism for ammonia detoxification as it facilitates the synthesis of urea and glutamine. Moreover, it offers a theoretical foundation for addressing the negative effects of chronic ammonia exposure in aquaculture.
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